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Biomedical subjects

A Alfaro

Publications and source records attributed to A Alfaro.

At least 19 recordsLinked to original sources
PubMed1996

Hemidiaphragmatic paralysis caused by cervical herpes zoster.

Although herpes zoster virus usually affects sensory nerves, it can also damage motoneurons. Injury to the phrenic nerve has been described previously, but only anecdotally. We report on a case of left hemidiaphragmatic paralysis with severe axonal degeneration secondary to cervical herpes zoster, and describe its clinical, radiological, pulmonary function and electromyographic evolution during an 18-month follow-up.

Acyclovir↗
PubMed1994

Progressive bleeding in spontaneous thalamic hemorrhage.

Progressive bleeding is uncommon in spontaneous intracerebral hemorrhage. We describe two cases of spontaneous thalamic hemorrhage with evidence of active bleeding or rebleeding detected by noncontrast CT. The first patient was a 47-year-old man with a history of hypertension and cocaine abuse. The second patient, a 73-year-old man, had no valuable risk factors. It is noteworthy that most well-documented instances of continued bleeding or rebleeding in spontaneous intracerebral hemorrhage occur in the thalamus. The natural evolution of spontaneous intracerebral hemorrhage after the first hours of stroke remains to be elucidated.

Aged↗
PubMed1994

[Subdural hemorrhage of aneurysmal origin].

Although most subdural hematomas are considered to be venous in origin, they may also be of arterial origin. When subdural bleeding is due to the rupture of an intracranial aneurysm, most commonly at the middle cerebral or internal carotid arteries, the amount of subdural blood is usually small and of no clinical importance. We describe two patients with subdural hematomas secondary to rupture of an intracranial aneurysm, who needed prompt surgical treatment. The first patient had a left internal carotid artery aneurysm at the origin of the ophthalmic artery. In the second patient the aneurysm was at the anterior communicating artery and rebled into the subdural space directly through a right intraparenchymatous frontobasal hematoma. The most probable mechanism of subdural bleeding in our two patients was the existence of adhesions between the aneurysm and the arachnoid due to previous minor hemorrhages. The indication of cerebral angiography in a patient with subdural hematoma is based mainly upon the existence of meningeal signs, the presence of blood in more than one intracranial compartment or the rapid progression of bleeding.

Aged↗
PubMed1993

[Striatocapsular infarct in a young patient with heterozygous familial hypercholesterolemia and Klinefelter's syndrome].

Familial hyperlipidemia has received little attention as a possible cause of stroke in young patients. Some recent studies have demonstrated that lipoprotein (a) is a key factor for atherogenesis in familial hypercholesterolemia. Hypogonadism may also contribute to the elevation of serum lipids, but their influence as a risk factor for stroke is still less understood. A 34-year-old patient with heterozygous familial hypercholesterolemia presented with a left pure motor hemiparesis secondary to a right striatocapsular infarction. Arteriography showed atherosclerotic lesions in both internal carotid arteries. High levels of cholesterol, cLDL, apo B, and lipoprotein (a) were found. Clinical signs of hypogonadism were present and the karyotype led to the diagnosis of Klinefelter's syndrome (47,XXY). The early clinical course was excellent, and the levels of serum lipids were normalized with diet, lipid-lowering drugs and androgens. The importance of hyperlipidemia as a risk factor for stroke in the young, specially when it occurs in the context of familial hypercholesterolemia with elevated lipoprotein (a) levels, as well as the possible contribution of hypogonadism to the development of accelerated atherosclerosis in young patients, are discussed upon.

Adult↗
PubMed1993

Recurrent idiopathic trigeminal sensory neuropathy.

Idiopathic trigeminal neuropathy is a rare disorder characterized by transient sensory disturbances in the territory of one or more branches of the trigeminal nerve. Acute and chronic forms of the disease have been recognized, but to our knowledge no recurrent cases have been reported. Two cases of recurrent idiopathic trigeminal sensory neuropathy are reported. The patients presented sensory alterations limited to the territory of the trigeminal nerve in the absence of other clinical features. In both cases sensory disturbances began in the tongue and lips and later spread throughout the face. The whole trigeminal nerve territory was involved in the first patient, but in the second patient only the second and third trigeminal branches were affected. There was no muscle weakness or pain, and the corneal reflex was present in both patients. The first patient recovered completely after 3 months, but the symptoms recurred in a similar fashion 3 years later. In the second patient the symptoms occurred each winter for more than 10 years. The conditions in these two patients could be considered as recurrent idiopathic forms of trigeminal sensory neuropathy.

Adult↗
PubMed1992

Idiopathic trigeminal sensory neuropathy.

Idiopathic trigeminal sensory neuropathy is a rare disorder characterized by transient sensory disturbances in the territory of one or more branches of the trigeminal nerve. Acute and chronic forms of the disease have been recognized, but the boundaries between these groups are not clearly defined. Six cases of idiopathic trigeminal sensory neuropathy are reported. All patients presented with sensory abnormalities limited to the territory of one trigeminal nerve, in the absence of other clinical features. The symptoms were on the left side of the face in five cases and on the right side in one. No bilateral involvement was seen. There were no cases of muscle weakness, and the corneal reflex was always present. In two cases, sensory disturbances began in the tongue or lips and later spread through the entire territory of the three trigeminal branches. Both patients recovered completely after 3 months. The other four patients had involvement of the second and third branches (two cases), or the third branch alone (two cases), and the symptoms persisted unmodified for 2 to 4 years. There were no clinical variables at onset to enable one to predict an acute or chronic evolution of the disease.

Adult↗
PubMed1991

[Mumps encephalitis in adulthood].

Mumps virus is one of the most common causes of viral meningitis. Although brain involvement has been observed in a low proportion of children with mumps meningitis, a pure form of mumps encephalitis is extremely uncommon in the adult. A 23 year-old man presented with a rapidly evolving syndrome of cephalalgia , vomiting, mutism, disorders of gait, somnolence and dystonic movements. The electroencephalogram showed a diffusely slowed background activity. The CSF contained no cells, but the total protein concentration was elevated. The patient recovered without sequelae, but severe intellectual and motor disturbances persisted during more than a month. Serological studies showed an increase of blood IgM mumps-specific antibodies. We conclude that mumps encephalitis, although infrequent, should be considered among viral diseases that mimic herpes simplex encephalitis in the adulthood.

Adult↗